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Flashcards in Chapter 2 Deck (58):
1

Totipotent Stem Cell

cell that can become any cell or organism

-first 8 cells of zygote are totipotent

2

Pluripotent Stem Cell

cell that become any cell in the body, BUT NOT an organism

-Embryonic Stem Cells
-Blastocyst of the Zygote

3

Multipoint Stem Cell

cell that can differentiate into multiple different cell types, least amount between toti/pluripotent

4

Stem Cell

cells that have the ability to renew and differentiate

-when divided, produce one stem cell and one differentiated cell

5

Progenitor Cell

cells in between stem cells and differentiated cells

6

Three Germ Layers

Ectoderm-skin
Endoderm-inner linings of organs
Mesoderm-muscle

formed from pluripotent cells in the blastocyst

7

Labile Cells

cells that have the ability to divide rapidly and constantly (ex. skin cells)

8

Stable Cells

cells that can divide when necessary, but hang out in the Go phase (ex. inflammatory cells)

9

Permanent

post-unitotic, can't divide, permanently in Go

10

Ways that Cells can become injured:

pathogens (virus, bacteria
lack of oxygen
physical, chemical, thermal
radiation
toxins
inflammation
lack of nutrients
genetic defects
trauma
aging

11

Hypoxia and Anoxia

Hypoxia: lack of enough oxygen in cells
Anoxia: no oxygen getting to cells

-reversible if O2 restored
-due to: lack of O2 in air, decreased oxygen transport to cells (most common, ex. low BP)
-suffocation/drowning
-different cell types can survive w/o oxygen for different time lengths

12

Hypoxia Pathogenesis

lacks oxygen, electron transport chain clown down, reduces ATP production

all cells need ATP to function
Na/K pump failure: Hydropic Change (cells fill with water and explode because water follows salt)

Anaerobic metabolism
-increased Lactic Acid, change in pH

13

Chronic Injuries

Intracellular Accumulations
-cholesterol, misfolded proteins, pigments (lipofuscin), fat, etc.
Altered Growth and Differentiation

14

Acute Mild Injury

visible, reversible changes
-hydropic change
-steatosis

15

Atrophy

shrinkage, decrease in cell size

due to aging, lack of nutrients or hormones

16

Hypertrophy

increase in cell size

-due to hormonal stimulation
-increased functional demand (resistance training)
-results in increased protein synthesis in cells

17

Hyperplasia

increase in cell number

due to: hormonal stimulation, increased functional demand, chronic stress

results is increased cell division

ex. fat and callouses

18

Metaplasia

replacement of one cell type with another

most common in epithelial cells
reversible if stress removed

19

Dysplasia

change in cell, resulting in abnormal cell size, shape, or organization

Premalignant: surgery before cells are cancerous

20

Apoptosis

Programmed cell death

-unwanted tissue
-worn out cells
-Caspase activation
-doesn't affect nearby cells

21

Necrosis

pathological cell death

affects nearby cells
cells swell and rupture
inflammation results

22

Coagulative Necrosis

cells have died, but cell shape/architecture remains

"ghost cells"

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Liquefactive Necrosis

Complete dissolution of necrotic tissue

no traces left of recently dead cells
massive infiltration of neutrophils

24

Caseous Necrosis

accumulation of amorphous (no structure) debris within area of necrosis

associated with tuberculosis

25

Fat Necrosis

Fat tissue
damaged cells release lipase (which breaks down triglycerides)
released fatty acids react with calcium, forming chalky white areas

26

Inflammation

the local response to injury

-neutralized harmful agents
-removes dead tissue
-local and acute
initial response is vascular

27

Neutrophils

-most numerous white blood cell
-also referred to as polymorphonuclear neutrophils (PMNs)
-predominant in early inflammatory response (acute inflammation)
-phagocytic (ingest bacteria, dead cells, and cellular debris)

28

Monocytes/Macrophages

-white blood cell
-monocyte is immature macrophage
-very large cells
-phagocytic
-job is to clean up the rest of the cell
-associated with chronic inflammation

29

Lymphocytes

T cells
chronic inflammation

30

Cytokine

substances secreted by certain cells of the immune system that have an effect on other cells (in this case, increasing inflammation)

31

Paracrine
Autocrine
Endocrine/Hormone

Paracrine--to a neighboring cell
Autocrine--to the same cell
Endocrine/Hormone--in the blood

32

The Clotting System

-type of plasma-derived molecular mediator
-forms fibrinous meshwork at inflamed site
-keeps foreign bodies at the site of greatest inflammatory cell activity
-forms clot
-provides framework for repair and healing
-main substance is fibrin

33

The Complement System

-activates or collaborates with every other component of the inflammatory response (protein cascade)
-made in liver

34

The Kinin System

-functions to activate and assist inflammatory cells
-primary kinin is bradykinin
-causes vasodilation

35

Cell-Derived Molecular Mediator of Inflammation

Vasoactive Amines including Histamine and Serotonin
-functions: vasodilation and vascular permeability
-Arachidonic Acid

36

Arachidonic Acid

-long fatty acid, phospholipid
-Leukotrienes = Vascular Permeability
-Prostaglandins = Vasodilation

37

Vascular Stage of Acute Inflammation

-brief vasoconstriction, then vasodilation (changes in endothelial cells necessary so neutrophils can get through)
-increased blood flow
-mediated by: Histamine and Bradykinin
-capillaries become more permeable, allowing exudate to escape into tissues

38

Cellular Reaction Following Vascular Stage in Acute Inflammation

-leukocytes enter injured area
-adhesive proteins such as selectins and integrins allow neutrophils to attach to endothelial cells
-Diaspedis: cells crawl through endothelial cells
-neutrophils follow chemoattractants (Pac Man)
-Neutrophil Chemotaxis (Mast Cells)

39

4 Cardinal Signs of Inflammation

Tumor (swelling )

Rubor (redness)

Calor (heat)

Dolor (pain)

40

Exudate

Fluid/Cells that seep out of vessel or organ

-inflammatory exudate: accumulation of fluid and WBCs

41

Serous Exudate

-large amounts of watery fluid, low in proteins and inflammatory cells
-blister fluid
-joint swelling in rheumatoid arthritis

42

Fibrinous Exudate

-severe
-high vascular permeability (fibrinogen into tissues)
-scabs

43

Suppurative Exudate

-liquedative necrosis
-pus (empyema = pus in body cavity)
-lots of neutrophils

44

Chronic Inflammation

-T Lymphocytes (T-cells), macrophages
-persistent injury
-unsuccessful acute inflammatory response (not always)

45

Macrophage

WBCs that accumulate in a damaged area and release inflammatory mediators

-granulomatous inflammation (trying to wall off foreign invaders)

46

Lymphatic Effects of Inflammation

Lymphangitis: red streaks usually due to infection

Lymphadenis: enlarged tender lymph nodes

Lymphadenopathy: tender lymph nodes all over the body

47

Pyrogen

a substance, usually introduced by a bacteria, that produces fever when introduced or released in the blood

Endogenous: inside body causing fever
Exogenous: outside body causing fever

48

Laboratory Indicators of Inflammation

-C-reactive protein
-Erythrocyte Sedimentation Rate (ESR)
------how fast RBC settle to the bottom of tube (because clotting factors attached to blood cells)

49

Regenerate
Healing
Fibrinous Repair

regenerate--near complete restoration
healing--regeneration and scarring
fibrinous repair--scar formation

50

Three different Phases of Wound Healing

Phase I: Inflammation
Phase 2: Proliferative
Phase 3: Remodeling and Maturation

51

Proliferative Phase

-cells migrate into wound
-Macrophages clean up and secrete growth factors (vascular, epithelial, etc.)

Angioblasts: cells that form new capillaries

52

Granulation Tissue

during the proliferative phase, tissue that grows into the wound from surrounding healthy connective tissue (temporary)

duration dependent on size and location of wound

53

Angiogenesis

growth of new blood vessels into wound

stimulated by vascular endothelial growth factor (brought by macrophages)

54

Fibroplasia

increase in fibroblast production during proliferative phase, which produce collagen, increasing the wound's strength

55

Epithelialization

epithelial cells migrating to wound to form barrier between wound and environment during the proliferative phase

56

Primary vs. Secondary Intention

during Phase III: Remodeling and Maturation

primary = wounds that heal under conditions of minimal tissue loss
secondary = wounds that require a great deal more tissue replacement

57

Three Host factors interfering with wound healing

Vitamin C: needed for collagen synthesis
Protein
Vitamin A: stimulates and supports epithelial cells

58

Dehiscence

wound pulls apart due to tension